FIGURE

Fig. 4

ID

ZDB-FIG-101105-48

Publication

Butler et al., 2010 - Genetic and chemical modulation of spastin-dependent axon outgrowth in zebrafish embryos indicates a role for impaired microtubule dynamics in hereditary spastic paraplegia

Other Figures

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Fig. 4

Nocodazole does not ameliorate the effect of reduced spast activity on spinal motor axon outgrowth. Embryos were microinjected with 0.4 pmol of spg4atg1 morpholino and continuously exposed to nocodazole at the concentrations indicated from 24 hpf to 30 hpf, prior to fixation and immunostaining with znp-1. Representative images are shown of an untreated uninjected embryo (A); an uninjected embryo treated with 0.5 μg/ml nocodazole (B); a spast-morphant embryo treated with DMSO vehicle (C); a spast-morphant embryo treated with 0.1 μg/ml nocodazole (D); a spast-morphant embryo treated with 0.3 μg/ml nocodazole (E); and a spast-morphant embryo treated with 0.5 µg/ml nocodazole (F). Scale bars: 50 μm.

Expression Data

Antibody:	znp-1
Fish:	WT WT + MO1-spast
Knockdown Reagent:	MO1-spast
Anatomical Terms:	motor neuron axon spinal cord motor neuron
Stage:	Prim-5

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	WT + MO1-spast
Knockdown Reagent:	MO1-spast
Observed In:	axon extension motor neuron axon
Stage:	Prim-5

Phenotype Detail

Acknowledgments

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